Thyroid function and hyperfunction during gestation

FOLLOWING implantation, a series of hormonal and metabolic events occur that help to shield the fetus from unfavorable changes in the maternal environment. From an endocrine standpoint these changes are controlled by steroid production in the fetal adrenals and gonads and in the placenta, as well as polypeptide hormones produced by the fetal pituitary and placenta. There is a constant hormonal interplay among fetus, mother, and placenta during pregnancy. Human CG (hCG) concentrations rapidly increase ensuring a supply of progesterone necessary for the maintenance of pregnancy before placental production is assured. These endocrine changes, including chorionic somatomammotropin production, also alter fuel metabolism, perhaps ensuring substrate for fetal growth (1). Serum PRL levels increase as do levels of CRH as a result of pituitary and hypothalamic stimulation (2). Maternal blood volume increases by 40% above nonpregnant values due to hormonal changes and venous distension that occurs when the vascular capacity of the uterus is increased. As a consequence, serum proteins, like albumin, undergo a relative decrease. Cardiac output, stroke volume, and heart rate are all increased in the pregnant woman, and systemic resistance is decreased (3). In the kidney of the pregnant woman, renal blood flow increases and the glomerular filtration rate may be increased by as much as 50% (4).